EFFECT OF VITAMIN K1 ON GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENT NEONATAL ERYTHROCYTES IN VITRO

Aim—To determine whether vitamin K1, which is routinely administered to neonates, could act as an exogenous oxidising agent and be partly responsible for haemolysis in glucose-6-phosphatdehydrogenase (G-6-PD). Methods—G-6-PD deficient (n=7) and control (n=10) umbilical cord blood red blood cells were incubated in vitro with a vitamin K1 preparation (Konakion). Two concentrations of Vitamin K1 were used, both higher than that of expected serum concentrations, following routine injection of 1 mg vitamin K1. Concentrations of reduced glutathione (GSH) and methaemoglobin, indicators of oxidative red blood cell damage, were determined before and after incubation, and the mean percentage change from baseline calculated. Results—Values (mean (SD)) for GSH, at baseline, and after incubation with vitamin K1 at concentrations of 44 and 444 µM, respectively, and percentage change from baseline (mean (SD)) were 1.97 + 0.31 µmol/g haemoglobin, 1.89 ± 0.44 µmol/g (-4.3 ± 13.1%), and 1.69 ± 0.41 µmol/g (-14.5 ±9.3%) for the G-6-PD deficient red blood cells, and 2.27 ± 0.31 µmol/g haemoglobin, 2.09 ± 0.56 µmol/g (˛7.2 ± 23.2%), and 2.12 ± 0.38 µmol/g (˛6.0 + 14.1%) for the control cells. For methaemoglobin (percentage of total haemoglobin), the corresponding values were 2.01± 0.53%, 1.93 ± 0.37% (˛0.6 ± 17.4%) and 2.06 ± 0.43% (5.7 ± 14.2%) for the G-6-PD deficient red blood cells, and 1.56 ± 0.74%, 1.70 ± 0.78% (12.7 ± 21.9%), and 1.78 ± 0.71% (20.6 ± 26.8%) for the control red blood cells. None of the corresponding percentage changes from baseline was significantly diVerent when G-6-PD deficient and control red blood cells were compared. Conclusions—These findings suggest that G-6-PD deficient red blood cells are not at increased risk of oxidative damage from vitamin K1. (Arch Dis Child Fetal Neonatal Ed 1998;79:F218‐F220)